RAD7 homologues contribute to Arabidopsis UV tolerance

Abstract

Frequent exposure of plants to solar ultraviolet radiation (UV) results in damaged DNA. One mechanism of DNA repair is the light independent pathway Global Genomic Nucleotide Excision Repair (GG-NER), which repairs UV damaged DNA throughout the genome. In mammals, GG-NER DNA damage recognition is performed by the Damaged DNA Binding protein 1 and 2 (DDB1/2) complex which recruits the Xeroderma Pigmentosa group C (XPC) / RAD23D complex. In the yeast Saccharomyces cerevisiae, distinct proteins, Radiation sensitive 7 and 16 (Rad7p and Rad16p), recognize the damaged DNA strand and then recruit the XPC homologue, Rad4p, and Rad23p. The remainder of the proteins involved GG-NER are well conserved. DDB1, DDB2, XPC/RAD4, and RAD23 homologues have been described in the model plant Arabidopsis thaliana. In this study we characterize three Arabidopsis RAD7 homologues, RAD7a, RAD7b, and RAD7c. Loss of function alleles of each of the three RAD7 homologues result in increased UV sensitivity. In addition, RAD7b and RAD7c overexpression lines exhibited increased UV tolerance. Thus RAD7 homologues contribute to UV tolerance in plants as well as in yeast. This is the first time any system has been shown to utilize both the DDB1/2 and RAD7/16 damage recognition complexes.